Zuo Qingting, Lyu Jiayan, Shen Xinran, Wang Fengju, Xing Liyun, Zhou Minglu, Zhou Zhou, Li Lian, Huang Yuan
Key laboratory of Drug Targeting and Drug Delivery System (Ministry of Education), West China School of Pharmacy, Sichuan University, No. 17, Block 3, South Renmin Road, Chengdu, 610041, P.R. China.
Small. 2024 Jun;20(25):e2307261. doi: 10.1002/smll.202307261. Epub 2024 Jan 15.
Conventional photodynamic therapy (PDT) of rheumatoid arthritis (RA) faces a dilemma: low-power is insufficient to kill pro-inflammatory cells while high-power exacerbates inflammation. Herein, mitochondrial targeting is introduced in PDT of RA to implement a "less-is-more" strategy, where higher apoptosis in pro-inflammatory cells are achieved with lower laser power. In arthritic rats, chlorine 6-loaded and mitochondria-targeting liposomes (Ce6@M-Lip) passively accumulated in inflamed joints, entered pro-inflammatory macrophages, and actively localized to mitochondria, leading to enhanced mitochondrial dysfunction under laser irradiation. By effectively disrupting mitochondria, pro-inflammatory macrophages are more susceptible to PDT, resulting in increased apoptosis initiation. Additionally, it identifies that high-power irradiation caused cell rupture and release of endogenous danger signals that recruited and activated additional macrophages. In contrast, under low-power irradiation, mitochondria-targeting Ce6@M-Lip not only prevented inflammation but also reduced pro-inflammatory macrophage infiltration and pro-inflammatory cytokine secretion. Overall, targeting mitochondria reconciled therapeutic efficacy and inflammation, thus enabling efficacious yet inflammation-sparing PDT for RA. This highlights the promise of mitochondrial targeting to resolve the dilemma between anti-inflammatory efficacy and inflammatory exacerbation in PDT by implementing a "less-is-more" strategy.
类风湿性关节炎(RA)的传统光动力疗法(PDT)面临两难境地:低功率不足以杀死促炎细胞,而高功率会加剧炎症。在此,将线粒体靶向引入RA的PDT中以实施“少即是多”策略,即使用较低激光功率在促炎细胞中实现更高的细胞凋亡。在关节炎大鼠中,负载氯6并靶向线粒体的脂质体(Ce6@M-Lip)被动积聚在发炎关节中,进入促炎巨噬细胞,并主动定位于线粒体,导致激光照射下线粒体功能障碍增强。通过有效破坏线粒体,促炎巨噬细胞对PDT更敏感,导致凋亡起始增加。此外,研究发现高功率照射会导致细胞破裂并释放内源性危险信号,从而招募并激活更多巨噬细胞。相比之下,在低功率照射下,靶向线粒体的Ce6@M-Lip不仅能预防炎症,还能减少促炎巨噬细胞浸润和促炎细胞因子分泌。总体而言,靶向线粒体协调了治疗效果和炎症反应,从而实现了对RA有效且不加重炎症的PDT。这凸显了通过实施“少即是多”策略,线粒体靶向有望解决PDT中抗炎疗效与炎症加剧之间的两难问题。